Although PGHS-2 expression and activity is enhanced in various pathophysiological conditions, such as preeclampsia, hypertension, and ageing (reviewed in [51]), previous research demonstrated an essential role of PGHS-2 in postnatal CV maturation (the transition of the cardiopulmonary circulation at birth) [53] and in the maintenance of normal renal architecture (progression of the renal dysplasia seen in COX (PGHS)-2–deficient mice) [54], and PGHS-2 downregulation has been shown to contribute to the development of kidney pathologies, due to intrauterine growth restriction [55]. Here, PTGS2 is linked to urogenital neoplasm.